ArticleOncoTargets and therapy2019
Expression of NR1H3 in endometrial carcinoma and its effect on the proliferation of Ishikawa cells in vitro.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Lipid metabolism reprogramming in endometrial cancer: biological functions and therapeutic implications.Cell communication and signaling : CCS · 2024Review
- Emerging Insights into Liver X Receptor α in the Tumorigenesis and Therapeutics of Human Cancers.Biomolecules · 2023Review
- Review
- Identification of Ten-Gene Related to Lipid Metabolism for Predicting Overall Survival of Breast Invasive Carcinoma.Contrast media & molecular imaging · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeOur study aimed to investigate the expression of NR1H3 in endometrial carcinoma, its effect on the proliferation of endometrial carcinoma cells in vitro, and the underlying mechanism of this effect. MATERIALS AND
methodsImmunohistochemistry of paraffin-embedded, sectioned specimens and of a tissue microarray was conducted to estimate the expression of NR1H3 (liver X receptors α: LXRα) and NR1H2 (liver X receptors β: LXRβ) in endometrial carcinoma tissues. The subcellular localization of NR1H3 in the endometrial carcinoma cell line Ishikawa was determined by immunofluorescence. An agonist of NR1H3, TO901317, was then administered to activate the expression of NR1H3, and cell viability and cell-cycle progression were investigated through MTT and flow cytometric assays, respectively. The gene and protein expression levels of NR1H3, cyclin D1 (CCND1), and cyclin E (CCNE) in cells pretreated with different concentrations of TO901317 for different periods of time were also detected by real-time RT-PCR and Western blot, respectively.
resultsThe results showed that, in contrast to NR1H2, which was expressed at low levels in endometrial tissues, NR1H3 was upregulated in endometrial adenocarcinoma tissues compared to levels in normal endometrial tissues and endometrial polyps. Moreover, NR1H3 was mainly expressed in the cytoplasm of Ishikawa cells. TO901317 significantly decreased cell viability and arrested the cell cycle in Ishikawa cells in a dose- and time-dependent manner. Furthermore, the administration of TO901317 not only promoted the expression of NR1H3 but also inhibited the expression of CCND1 and CCNE in Ishikawa cells.
conclusionWe demonstrated that NR1H3 is upregulated in endometrial adenocarcinoma and that it inhibits cell viability by inhibiting the expression of CCND1 and CCNE in endometrial carcinoma cells. Our study indicates that NR1H3 may play a role in the development of endometrial cancer and may emerge as a promising therapeutic target.
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